Evidence map›Paper›PMID 22884559›Full record

ArticlePhysiology & behavior2012

Exposure to dexamethasone during late gestation causes female-specific decreases in core body temperature and prepro-thyrotropin-releasing hormone expression in the paraventricular nucleus of the hypothalamus in rats.

David L Carbone, Damian G Zuloaga, Anthony F Lacagnina, Robert F McGivern, Robert J Handa

Abstract read
In one paragraph

Article in Physiology & behavior, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Prenatal dexamethasone programs autonomic dysregulation in female rats.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Sex differences in major depression and comorbidity of cardiometabolic disorders: impact of prenatal stress and immune exposures.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    Review
  7. Article
  8. Article
  9. Advances in TRH signaling.Reviews in endocrine & metabolic disorders · 2016
    Review
  10. Article
  11. Review
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

David L CarboneUniversity of Arizona College of Medicine-Phoenix, Department of Basic Medical Sciences, Phoenix, AZ 85004-2157, United States. carbone@email.arizona.edu
Damian G Zuloaga
Anthony F Lacagnina
Robert F McGivern
Robert J Handa
University of Arizona · USSan Diego State University · US

Funding

Sex-Specific Programming of the HPA Axis by GlucocorticoidsP50MH082679 · NIMH · BRIGHAM AND WOMEN'S HOSPITAL · PI GOLDSTEIN, JILL M · 2007 to 2011
$5.9M
SEX DIFFERENCES IN HYPOTHALAMO-PITUITARY-ADRENAL AXISR01NS039951 · NINDS · UNIVERSITY OF ARIZONA · PI HANDA, ROBERT J · 2001 to 2013
$4.3M
NIMH NIH HHS P50 MH082679NINDS NIH HHS R01 NS039951
6 · The paper itself

Abstract

Synthetic glucocorticoids (GC) have been used to promote lung development in preterm infants, thereby decreasing respiratory distress syndrome and mortality, yet, concern has arisen from reports that such treatment predisposes individuals to disease in adulthood. Given the variety of preclinical studies that show metabolic and behavioral abnormalities in adulthood following fetal exposure to synthetic GC, we examined the effect of in utero exposure to the synthetic GC, dexamethasone (DEX), on hypothalamic expression of thyrotropin-releasing hormone (TRH) a central neuropeptide involved in mediating behavior and metabolic balance. Pregnant Sprague-Dawley rats were administered 0.4mg/kg DEX on gestational days 18-21. As adults (postnatal day (PD) 60), the offspring were fitted with temperature sensing transmitters allowing real-time monitoring of core body temperature (CBT) across the 24h light dark period. This revealed a significant decrease in CBT throughout the day in prenatal DEX-treated females on estrus and diestrus, but not in male offspring. The reduction in CBT by prenatal DEX exposure was accompanied by a significant decrease in the expression of Trh transcript in the paraventricular nucleus of the hypothalamus (PVN) of female rats at PD 60 and this effect was also present on PD7. There was also a female-specific reduction in the number of preproTRH-immunoreactive (ir) neurons in the PVN, with ppTRH-ir nerve fibers decreases that were present in both male and female offspring. No changes in thyroid hormone (triiodothyronine, T3; thyroxine, T4) were observed in adult offspring, but during development, both males and females (PD14) had lower T3 and T4 levels. These data indicate abnormal expression of TRH results from fetal DEX exposure during late gestation, possibly explaining the decreased CBT observed in the female offspring.

Indexed as

Prenatal Exposure Delayed EffectsAge FactorsAnalysis of VarianceAnimalsAnimals, NewbornAnti-Inflammatory AgentsBody TemperatureCircadian RhythmDexamethasoneFemaleGene Expression Regulation, DevelopmentalGestational AgeParaventricular Hypothalamic NucleusPregnancyProtein PrecursorsRatsAnti-Inflammatory AgentsDexamethasoneprepro-thyrotropin-releasing hormoneProtein PrecursorsRNA, MessengerThyrotropin-Releasing HormoneThyroxineTriiodothyronine

Identifiers

PMID22884559
PMCPMC3513498
OpenAlexW2068179056

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.